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Ezh1 ul3/ul3 zebrafish mutants present a normal phenotype.
Ezh2-deficient zebrafish mutants present a normal body plan but die at around 12 dpf with defects in the intestine wall, due to enhanced cell death.
Mouse embryos lacking Ezh2 function fail to complete gastrulation27, but ezh2ul2/ul2 zebrafish mutants present a normal body plan and die at around 12 days post fertilization (dpf) with intestinal defects.
Because of their large numbers, embryo-defective mutants present a special challenge for saturation mutagenesis.
In S. cerevisiae, cda1 mutants present a more diffuse chitosan layer, while their surface layer remains intact.
Arabidopsis thaliana drb2 mutants present a 2 to 10 fold increase in RdDM associated p4-siRNA ([ 50] and Figure 1a) again suggesting that plant DRB2 is involved in regulating small RNA biogenesis and is therefore a regulator of RdDM.
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We also observed that the kinase-inactive mutants present an increased basal T-loop phosphorylation, modestly increased by hypotonic low chloride conditions.
Induction of AtCuAO1 by ABA has been previously observed by Wimalasekera et al. [ 21], who showed that cuao1 mutants present an ABA-hyposensitive phenotype and impaired H2O2 and NO production.
Three of the mutants presented a conditional-lethal phenotype in vitro.
A detailed analysis of the fragmentation of sleep revealed that Afh mutants presented a significantly higher number of NREM episodes compared to wild-type mice mainly in the dark phase (Supplementary Fig. S2a, Table 1), while the number of REM episodes was similar between the two genotypes (Supplementary Fig. S2b, Table 1).
However, 10 of the mutants (designated AM 1 10, meaning Adhesion or invasion defective Mutants) presented a higher than 50 % reduction in adherence in comparison to the adherence observed in the parent strain (Fig. 2).
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